EHRA/EAPCI expert consensus statement on catheter-based left atrial appendage occlusion - an update

The rationale for the quest to close the left atrial appendage (LAA) for stroke prevention is composed of three elements: the concept that atrial fibrillation (AF) causes strokes, the concept that strokes are associated with thrombus formation in the LAA, and that these thrombi cause strokes by embolisation to the cerebral circulation. There are strong data supporting an association between AF and stroke. The Framingham study following 5,070 patients over 34 years demonstrated an approximately fivefold higher stroke risk in individuals with AF than in those without.1 Though this does not prove a causal relationship, it is important to mention that this risk remained even after adjustment for other risk factors such as hypertension, coronary artery disease, congestive heart failure, and age. Another element to support LAA closure is that there must be proof that thrombus formation occurs predominantly in the LAA. One would imagine that there are abundant data to support the concept that, in AF, thrombus formation occurs predominantly in the LAA; however, in almost all texts discussing the pathophysiology of stroke in AF there are few publications cited to support this concept. Blackshear et al included 1,288 patients with non-valvular AF who underwent either transoesophageal echocardiography (TOE) or autopsy. 2 Thrombus formation was reported in 222 patients, 91% of which was located in the LAA. It was further supported by a more comprehensive meta-analysis by Mahajan et al who demonstrated that 89% of thrombi in the left atrium (LA) were located in the LAA.3 This was corroborated by a study in the realm of degenerative aortic stenosis by Parashar et al.4 In this study, all left atrial thrombi resided in the LAA. It is worth mentioning that the LAA is the most common site of intracardiac thrombi not only in patients with AF but also in patients in sinus rhythm.5 More direct evidence is now available proving that a large proportion of strokes in AF are the result of thrombus in the LAA. The PROTECT AF and PREVAIL studies (described later in this document) provide evidence for the protective effect of LAA closure on thromboembolic events (Chapter 5), although some have debated the evidence (Chapter 6).6 In order to justify LAA closure it is important to show that, when thrombus occurs in the LAA, it can embolise in the cerebral circulation. o demonstrate this, a thrombus embolising to the brain would have to be caught in the act. Parekh et al describe real-time imaging capture of LAA thrombus embolisation during TOE with subsequent stroke after a delay of 4 hours of the witnessed embolisation, possibly due to initial retention at a non-occlusive location with subsequent fragmentation and delayed more distal embolisation.7 The fact that LAA closure prevents thromboembolic events as detailed above is also indirect proof for embolisation from LAA as a cause of embolic events.